BACKGROUND:Qing-Fei-Yin Decoction (QFY), derived from the classical formula Ma-Xing-Shi-Gan Decoction, emphasized "clearing heat and detoxifying, ventilating the lungs, and relieving cough," has been widely used for the treatment of influenza and has demonstrated significant efficacy. However, the studies on its mechanism were limited. OBJECTIVE:This study aimed to systematically evaluate its efficacy and explore its action mechanism using murine model of influenza. METHODS:The chemical profile of QFY was analyzed using UPLC-MS. A murine model challenged by PR8 (H1N1) influenza virus was established with C57BL/6J mice. Mice were randomly assigned to QFY-treat, oseltamivir-treat, PBS-treat, control groups. Multiple indicators (including survival rate, pathological alteration of lungs and colon, viral load, and inflammatory cytokine levels in lung and serum) were assessed. In addition, transcriptomic sequencing of lung tissues and 16S rRNA sequencing of gut microbiota were conducted. RESULTS:QFY improved the 14-day survival rate of infected mice from 0 % (PBS group) to 40 %, though still below the 60 % observed in the oseltamivir group. It alleviated lung pathological injury, reduced viral load, and downregulated pro-inflammatory cytokines (TNF-α, IL-6, IFN-γ, CCL2, CXCL10). Transcriptomic analysis of lung tissue revealed that QFY markedly suppressed the activation of NF-κB, TNF, IL-17, and NOD-like receptor signaling pathways, while enhancing the expression of genes related to epithelial barrier function. Furthermore, QFY restored gut microbiota homeostasis, increasing beneficial microbiota such as Barnesiella, which promotes short-chain fatty acid production, while inhibiting the overgrowth of pathogenic genera like Escherichia. CONCLUSION:QFY Decoction exhibited experimentally validated anti-influenza activity, mediated primarily through three mechanisms: inhibition of viral replication, suppression of excessive inflammation, and modulation of intestinal microbiota balance.

Multidrug-resistant Klebsiella pneumoniae (MDR-KP) infections present a global health crisis, with escalating resistance to last-line antibiotics. Traditional Chinese medicines (TCMs) demonstrate multi-component synergy against resistant pathogens. This study deciphered the antibacterial mechanisms of bioactive TCM components targeting MDR-KP through integrative pharmacology and experimental validation. Four core TCMs (Scutellaria baicalensis, Forsythia suspensa, Lonicera japonica, Aloe vera) were screened via Chinese Pharmacopoeia and TCMSP database. Network pharmacology identified core components and enriched pathways. Clinically isolated MDR-KP strains (resistant to meropenem, polymyxin E, and tigecycline) were characterized. Synergistic effects were evaluated using checkerboard assays, biofilm quantification, and membrane permeability assays. Molecular docking and RT-qPCR analyzed target interactions, while ELISA and CCK-8 assessed anti-inflammatory activity and cytotoxicity. Consequently, luteolin, wogonin, and kaempferol were identified as key components targeting PI3K/AKT and MAPK pathways. Their triple combination (2/4/8 μg/mL) exhibited potent synergy (FIC = 0.38), reducing biofilm biomass by 68

Objective: To investigate the mechanism of Fuzheng Jiedu Huayu Formula in alleviating lung injury in rats with multidrug resistant pseudomonas aeruginosa（MDRPA） chronic pneumonia by intervening NLRP3 inflammatory body.The rats were divided into the normal group, model group, Chinese medicine group, western medicine group, Chinese+western group randomly. The rat model of MDRPA chronic pneumonia was established by oral tracheal intubation. The Chinese medicine group was given Fuzheng Jiedu Huayu Formula by gavage, 1.4 g/mL per time, 2 times/d. The western medicine group was given piperacillin tazobactam sodium by intraperitoneal injection, q8 h. The Chinese+western group was given the two medicine.The pathological changes of lung tissues were observed at various time points. The expression of genes and proteins related to NLRP3 inflammatory body was observed by qPCR and Western blot. Results: Compared with the model group, the levels of NLRP3 mRNA and Caspase-1 mRNA in the Chinese medicine group decreased significantly on the 14th and 21st days（P＜0.05）,NLRP3 and IL-1β protein expression decreased significantly in the traditional Chinese medicine group, western medicine group and Chinese+western medicine group on the 14th day（P＜0.05）. Compared with the model group, the Chinese medicine group had more complete alveolar structure, less immune cell infiltration on the 7th and 14th days, and less immune cell infiltration and fibroblast formation on the 21st day. Conclusion: Fuzheng Jiedu Huayu Formula can significantly reduce the lung injury in rats with chronic pneumonia caused by MDRPA, which may play a role by regulating the expression of NLRP3 inflammatory body.

辛温药在古医籍中广泛应用于疫病的防治,而对辛温药治疫的机理缺少系统解读.中医学认为疫病病机为正气不足,外感毒邪,兼夹秽浊、热毒等而发病.本文参考古代本草著作,整理具有治疫作用的辛温药,从"辛能行散,温能助阳"的性味理论出发,归纳出辛温药在治疫过程中发挥温通阳气、消导阴浊、开通心窍功效.疫病病机复杂,种类多样,通过明晰辛温药治疫机理,在治疗中辨证地应用辛温药味,不断丰富和发展中医药治疫理论.

气一元论认为,气是构成世界万物的本原,也是构成人体和维持生命活动的基本物质.人禀气而生、得气以长,肺主一身之气的生成和运行,鼻为肺之外窍,是天地之气与人体之气相互交换的重要场所.通过梳理气一元论学说,发现过敏性鼻炎-哮喘综合征的发病机制与气的物质和功能属性密切相关,提出天地之气未顺、人气失调,导致气机失衡、痰饮内停是过敏性鼻炎-哮喘综合征的重要病机.其中,天地之气未顺是发病外因,人气失调是发病根本且受天地之气影响,气机失衡、痰饮内停是发病的关键环节.

哮喘是遗传和环境等多方面因素共同作用引发的疾病,哮喘的反复发作是治疗的难点与关键所在.《素问·刺法论篇》云"正气存内,邪不可干",提出了扶正祛邪的防病治病理念.从中医理论来讲,哮喘患者普遍存在肝肾不足的病理基础,其中肾虚精亏则易感寒邪、痰饮内生;肝血不足、水不涵木则易生风邪、上逆犯肺,二者是哮喘的重要病机.我们在临床中发现,即使在哮喘急性发作期亦应重视补益肝肾之法的应用,慢性持续期、缓解期更当以补益肝肾为立方之基,在重视补益肝肾的同时,不忘祛邪,并根据哮喘的不同阶段及兼夹证特点,结合体质、季节等,分期论治、随证加减,有望达到缩短病程、减少急性发作次数乃至治愈的目的.

Ethnopharmacological relevance: The combined prescription of two classical decoctions (Ma-Xing-Shi-Gan decoction with Xiao-Chai-Hu decoction), named as San-Yang-He-Zhi (SYHZ) decoction, has been widely used for the treatment of influenza virus (IFV) infections for decades.Aim of the study: This study aimed to evaluate the anti-influenza effect of SYHZ decoction and explore the un-derlying mechanism. Materials and methods: The ingredients of SYHZ decoction were analyzed by mass spectrometry. An animal model of IFV infection was established by challenging C57BL/6J mice with PR8 virus. Three groups of mice were infected with lethal or non-lethal doses of IFV, then followed by oral administration of phosphate-buffered saline (PBS), or SYHZ, or oseltamir; blank control mice (without IFV infection) were treated with PBS. Survival rate, Lung index, colon length, body weight loss and IFV viral load were measured 7 days post infection; histology and electron-microscopy examinations of lung tissue were performed; cytokine and chemokine levels in lung and serum were measured; and the intestinal metagenome, the cecum metabolome, and the lung transcriptome were analyzed. Results: SYHZ treatment significantly improved survival rate compared with PBS (40% vs 0%); improved lung index, colon length, and body weight loss; and alleviated lung histological damage and viral load. SYHZ-treated mice had significantly lower levels of IL-1 beta, TNF-alpha, IL-6, CCL2, CXCL10 in lung and serum, and increased levels of multiple bioactive components in cecum. Pro-inflammatory cytokines, Toll-and NOD-like receptors, pro-apoptosis molecules, and lung-injury-related proteins were downregulated in SYHZ mice, whereas surfactant protein and mucin were upregulated. The NOD-like receptor pathway, Toll-like receptor pathway, and NF-kappa B pathway were downregulated by SYHZ treatment.Conclusions: SYHZ decoction alleviated IFV infection in a mouse model. Multiple bioactive ingredients of SYHZ may inhibit replication of IFV and suppress excessive immune response.

Multidrug-resistance (MDR) Pseudomonas aeruginosa (P. aeruginosa) is a lethal gram-negative pathogen causing hospital-acquired and ventilator-associated pneumonia, which is difficult to treat. Our previous studies confirmed that baicalin, an essential bioactive component in Scutellaria baicalensis Georgi, exhibited anti-inflammatory effects in an acute pneumonia rat model induced by MDR P. aeruginosa. However, this effect of baicalin in constrast its low bioavailability, and its mechanism of action is still unknown. Thus, this study investigated whether the therapeutic effects of baicalin against MDR P. aeruginosa acute pneumonia are owing to the regulation of gut microbiota and their metabolites using pyrosequencing of the 16S rRNA genes in rat feces and metabolomics. As a result, baicalin attenuated the inflammation by acting directly on neutrophils and regulated the production of the inflammatory cytokines TNF-α, IL-1β, IL-6, and IL-10. The mechanisms were through down-regulation of TLR4 and inhibition of NF-κB. Furthermore, pyrosequencing of the 16S rRNA genes in rat feces revealed that baicalin regulated the composition of gut microbial communities. At the genus level, baicalin efficiently increased the abundance of Ligilactobacillus, Lactobacillus and Bacteroides, but decreased the abundance of Muribaculaceae and Alistipes. Further, arginine biosynthesis was analyzed as the core pathway regulated by baicalin via combination with predicting gut microbiota function and targeted metabolomics. In conclusion, this study has demonstrated that baicalin relieved inflammatory injury in acute pneumonia rat induced by MDR P. aeruginosa via arginine biosynthesis associated with gut microbiota. Baicalin could be a promising and effective adjunctive therapy for lung inflammation caused by MDR P. aeruginosa infection.

Objective:To explore the mechanism of Ma-Xing Shi-Gan decoction combined with Xiao-Chai-Hu decoction (hereinafter referred to as " Sanyang combined treatment" ) in alleviating colon injury in mice infected with influenza virus by transcriptome sequencing technique.Methods:The mouse model of colonic injury caused by influenza virus was induced by intranasal drip of influenza A virus H1N1 suspension. The mice were divided into Control group, Model group, and Sanyang combined treatment (SCT) group. Model group and SCT group were fed with PBS and Ma-Xing Shi-Gan decoction combined with Xiao-Chai-Hu decoction respectively. Seven days later, the colon tissues of each group were taken, the colon length and pathological damage were observed, and the transcriptome was sequenced to screen the significantly different genes between the SCT group and model group for Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Set Enrichment Analysis(GSEA).Results:After the therapy with SCT, the length of the colon of mice was significantly improved and the pathological injury of the colon was reduced. There are 92 differentially expressed genes between the SCT group and the model group. GO analysis indicated that the differential genes were enriched in biological processes such as regulation of cytokine and chemokine production, inflammatory response, defense response, immune response, regulation of NF-κB inducing kinase(NIK)/Nuclear factor-κB(NF-κB) signal and Mitogen-activated protein kinase(MAPK) cascade, as well as cell components related to intestinal barrier such as brush border membrane, brush border and microvilli. KEGG analysis indicated that the differential genes were enriched in Toll-like receptor signaling pathway, intestinal immune network for IgA production, complement and coagulation cascade, and Peroxisome proliferator-activated receptor(PPAR) signaling pathway. GSEA indicated that the intestinal immune network for IgA production, PPAR signaling pathway, propionic acid metabolism and butyrate metabolism were significantly up-regulated after the intervention with SCT, while apoptosis and MAPK signaling pathway were significantly down-regulated.Conclusions:Sanyang combined therapy can protect the intestinal tract of mice infected with influenza virus mainly through immunity, inflammation and metabolism pathways.

刘奎为清代著名瘟疫学家,少时多病,官运不济,不为良相,则为良医.其代表作《松峰说疫》等医学论著,在继承《景岳全书》和《瘟疫论》的学术思想基础上加以发扬和深化,严格划分瘟疫范畴,创"三疫"学说;继承并发扬了《伤寒论》六经辨证的理念,首创"瘟疫六经治法";综"瘟疫统治八法",以解毒为要;同时领先于其他国家学者,较早地提出避瘟预防的有效措施.刘奎的疫病防治理念和方药方法,为传染病学奠定了坚实基础,对后世医家产生了深远影响,尤其对当今疫情防控有着重要的启迪意义.

"灰中有火"出自叶天士《温热论》,强调温病后期,患者体内往往尚有余火,治疗用药时应慎用温热之品,防止故病未已,新病复起.老年慢性肺系疾病患者,素有痰热,适逢辛甘厚味、环境燥邪、六淫火气、痰热内生等诱因,容易使邪热内伏,一旦误投,"正气转郁,反致热极",轻则病重,重则病死,该情况与"灰中有火"理论相一致.故在临床诊治时,提示该类患者应饮食有节、防妄补,治疗既不可一味猛攻,也不能一味进补,应观其脉证,随证治之,常用清补、慎用温补,主次兼施,结合"治上焦如羽,非轻不举"原则,避免闭门留寇,炉灰复燃.

重症治疗过程中，应用苦寒抗生素及清热解毒中药、输注大量寒凉液体，以及病房低温环境、持续给予寒凉肠内营养液、过用物理降温等，均可损伤患者阳气，尤易伤其中焦脾阳，加之重症监护室以老年患者居多，其本身常存在脾肾阳气虚衰状况。因此，固护阳气在重症疾病治疗中不可忽视。临床可以益气健脾温阳法作为重症患者固护阳气的基本治法，将之应用于脓毒性休克、急性呼吸窘迫综合征、低T3综合征、获得性衰弱等重症并发症的治疗，可取得较好疗效。

麻杏石甘汤起源于《伤寒论》,是新冠疫情使用的中药基础方剂,在抗疫中发挥极其重要的作用.针对的病机是外邪郁闭、痰热阻肺,用于治疗肺热喘嗽与温热类疾病,在治疗呼吸道感染、肺炎、慢性阻塞性肺疾病(COPD)、支气管哮喘等疾病疗效显著.临床应用治疗哮喘中生石膏多为麻黄的4倍,麻黄最佳剂量为24 g;肺炎的治疗中石膏用量多为麻黄的5倍,麻杏石甘汤发挥抗病毒、抗炎等药理作用的相关靶点包括白细胞介素-6(IL-6)、IL-17、肿瘤坏死因子(TNF)、促分裂原活化的蛋白激酶(MAPK)等.临床治疗疾病中与免疫调控(包括成熟的T淋巴细胞CD3+、CD4+、CD8+等)密切相关.现对麻杏石甘汤的古代文献、治疗肺系疾病量效、药理作用、现代基础及临床研究进行概述.总结现有研究不足,在以后的研究应侧重于中药复方指纹图谱、药效机制、标准汤剂和治疗疾病疗效评价的标准化等方面开展.

支气管哮喘属中医学"哮病"范畴,各代医家形成了"哮病宿痰内伏"的病机学说.王成祥教授认为,哮病骤发时,除了宿痰内伏,风邪亦是重要的致病因素,哮病急性发作既责之于肺脾亏虚、外感风邪,又因于肝脾失和、风痰内生,因此在治疗时,王教授制定了疏解外风、平息内风、复肺之宣降、调和肝脾以杜绝生痰之源的治疗4法,肺肝脾诸脏同治,显著地控制了患者的临床症状,减少患者再次发作频率,临床疗效良好.

目的:探讨清燥救肺汤联合吡非尼酮治疗特发性肺纤维化疗效及对患者肺纤维化指标、支气管肺泡灌洗液胰岛素样生长因子的影响.方法:将 96 例特发性肺纤维化患者采用随机数字表法分为对照组和观察组,各 48例.对照组给予吡非尼酮治疗,观察组则在对照组基础上联用清燥救肺汤.比较两组治疗效果,观察治疗前后两组患者的中医症候积分、肺纤维化指标[层粘蛋白(LN)、透明质酸(HA)和Ⅲ型前胶原(PC Ⅲ)]、支气管肺泡灌洗液胰岛素样生长因子[支气管肺泡灌洗液胰岛素样生长因子Ⅰ(IGF-Ⅰ)、胰岛素样生长因子结合蛋白(IGFBP-4)]水平和肺功能恢复指标[肺一氧化碳弥散量(DLCO)、第一秒用力肺活量(FEV1)和 6 min步行实验(6 MWD)],并统计两组不良反应发生率.结果:观察组临床治疗总有效率明显高于对照组(P＜0.05).两组治疗后气急喘促、咳吐浊唾、口渴咽干、手足心热和舌红脉虚数症候积分较治疗前显著降低,且观察组低于对照组(均P＜0.05).两组治疗后 LN、HA、PC Ⅲ、IGF-Ⅰ和 IGFBP-4 水平较治疗前显著降低,且观察组治疗后低于对照组(均P＜0.05).两组治疗后DLCO、FEV1、6MWD较治疗前显著升高,且观察组显著优于对照组(均P＜0.05).两组不良反应比较差异无统计学意义(P＞0.05).结论:清燥救肺汤联合吡非尼酮可有效缓解特发性肺纤维化患者肺纤维化程度,降低支气管肺泡灌洗液胰岛素样生长因子水平,提高肺功能,并改善阴虚肺燥症候,提高临床疗效,且未增加不良反应,安全性好.

目的 预测基于千金三黄汤加减的"麻黄-黄芩-黄芪-鱼腥草"配伍治疗甲型流感病毒感染的潜在作用靶点及作用机制,以期丰富抗流感病毒的复方配伍.方法 通过中药系统药理学分析平台数据库(TCMSP)、PubChem数据库、Swiss Target Prediction数据库筛选麻黄、黄芩、黄芪、鱼腥草的活性成分与潜在靶点.使用GeneCards数据库筛选流感病毒感染的疾病相关靶点,利用微生信平台中"集合运算Venn图"获得药物与甲型流感病毒的交集靶点.通过Cytoscape 3.8.2 软件构建"药物-活性成分-作用靶点"网络并进行拓扑分析.利用String数据库构建蛋白质-蛋白质互作(PPI)网络,并通过Cytoscape 3.8.2 软件进行拓扑分析,获得核心靶点.并应用Metascape数据库进行GO及KEGG富集分析.流感病毒PR8 构建C57BL/6J小鼠感染模型,观察小鼠一般状态、肺指数、肺组织病理,ELISA及RT-PCR对部分核心靶点及抑炎因子表达进行检测.结果 得到"麻黄-黄芩-黄芪-鱼腥草"配伍的活性成分 86 个,潜在靶点 505 个.甲型流感病毒相关的疾病靶点 1531 个.药物与疾病的交集靶点 175 个.GO富集获得424 个条目,KEGG通路富集获得 202 个条目,涉及PI3K-Akt信号通路、流感通路、COVID-19 通路、C型凝集素受体信号通路、TNF信号通路、IL-17 信号通路、凋亡通路、Th17 分化等多个流感相关的通路.实验结果表明,中药干预后可以改善感染小鼠一般状态及感染诱发的结肠缩短,减轻肺指数与肺组织病理损伤,下调核心靶点中促炎因子 TNF-α、IL-6、MAPK3、IL-1βmRNA 的表达、上调抑炎因子IL-10的表达.结论 基于千金三黄汤加减的"麻黄-黄芩-黄芪-鱼腥草"配伍可以多成分、多途径发挥抗甲型流感病毒的作用,可能通过TNF-α、IL-6、MAPK3、IL-1β、Akt1 等核心靶点调控PI3K-Akt信号通路、TNF信号通路、IL-17 信号通路等减轻甲型流感病毒所致的肺组织免疫炎性损伤,初步证实了该配伍治疗甲型流感病毒感染的部分作用靶点及对感染小鼠的保护作用.

Influenza virus-caused lung infection and its pandemic outbreaks are a persistent public health challenge. The H1N1 subtype is the most common type of influenza infection observed in humans. Maxingshigantang decoction, a classic formula of Chinese herbal medicine, has been used for the prevention and treatment of respiratory infection for many centuries. Qingfeiyin decoction, based on Maxingshigantang, has been used in the clinic for decades. To explore the underlying mechanisms, according to the traditional Chinese medicine theory “the lung and the large intestine are interior–exterior,” which can be translated to the “gut–lung axis” in a contemporary term, the composition of gut microbiota was determined using 16S rRNA and the transcriptome of the colon was determined by RNA sequencing. The results showed that Qingfeiyin decoction decreased the viral load, alleviated the lung injury, increased the survival rate, partly restored the shortening of the colon caused by the H1N1 virus, and downregulated inflammatory pathways including MAPK, TNFα, and JAK-STAT signaling pathways. Qingfeiyin decoction increased the relative abundance of the genera of Coprococcus, Ruminococcus, Lactobacillus, and Prevotella and prevented the H1N1 virus-induced decrease in the abundance of the genera of Escherichia, Parabacteroides, Butyricimonas, and Anacrotruncus. These results will help better understand the mechanisms for Qingfeiyin decoction’s protective effect against influenza virus infection.

"芪银三两三"是中国著名呼吸病、热病专家周平安根据古代民间验方"外科疮疡三两三"去蜈蚣一药化裁而成,该方由生黄芪、金银花、当归、生甘草四味药物组成,具有益气活血、解毒愈疡的功效.周平安教授认为临床很多常见病、疑难杂症如过敏性鼻炎、过敏性哮喘、肺部结节、硬皮病、肺间质纤维化,其根本病机均在于正虚邪聚,正虚包括肺卫不固、肝血不足、阳气亏虚等,邪聚包括风盛、痰瘀、寒凝等,故周平安在治疗以上几类疾病时紧扣病机、异病同治,均以"芪银三两三"作为扶正祛邪的基础方,由点及面,配伍多种自拟经验方如柴胡脱敏汤、肺痹汤及多种药对等,同时将中药传统的四气五味与现代药理紧密结合,达到调肝理肺、化痰消癥、温阳荣肌、活血通痹之功,扩大了"芪银三两三"原有的临床应用范围.现将周平安应用"芪银三两三"的治疗经验归纳如下并对典型临床病案进行分析.

膈肌功能障碍是一种呼气和吸气时膈肌厚度变异率小于30％的临床诊断性疾病,是以喘促、脱机困难、膈肌厚度减低为特征的疾病.有创机械通气是膈肌功能障碍最常见原因,导致脱机困难,严重影响疾病预后,因此,探析有创呼吸机通气膈肌功能障碍的中医病机,对中医治疗该病的临床思路起着至关重要的作用.根据该病的临床表现可将其归于中医"喘证""痿病"范畴,肺脾肾虚是其主要病机,可依据补肺健脾益肾理论进行论治.

目的 研究黄芩苷对多重耐药铜绿假单胞菌(MDRPA)慢性肺部感染大鼠的影响.方法 将32只SPF级雄性SD大鼠(6～8周龄,体重180～220g)采用随机数字表法分为空白组、模型组、西药组和黄芩苷组,每组8只.其中模型组、西药组和黄芩苷组采用经口气管插管法注入MDRPA藻酸盐包被体建立MDRPA慢性肺部感染大鼠模型.黄芩苷组给予0.8g/(kg·d)黄芩苷灌胃,西药组给予0.8g/(kg·d)哌拉西林他唑巴坦钠肌肉注射;空白组、模型组均给予与黄芩苷组等量的生理盐水灌胃.干预14 d后留取四组血清和肺组织,采用苏木精-伊红染色观察肺组织;酶联免疫吸附试验检测血清中肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL-10)水平;实时定量聚合酶链反应检测肺组织Toll样受体4(TLR4)、核因子κB(p65亚基)(NF-κB p65)mRNA的表达.结果 空白组肺组织形态结构正常;模型组肺组织可见大量炎症细胞浸润,肺泡壁显著增厚;黄芩苷组肺组织浸润的炎症细胞较少,肺泡壁较薄.模型组血清TNF-α水平及肺组织TLR4、NF-κB p65 mRNA水平均高于空白组,血清IL-10水平低于空白组(P＜0.05).黄芩苷组血清TNF-α水平及肺组织TLR4、NF-κB NF-κB p65 mRNA水平均低于模型组,血清IL-10水平高于模型组(P＜0.05).结论 黄芩苷可以减轻MDRPA慢性肺部感染大鼠肺组织炎症损伤,其机制可能与抑制TLR4/NF-κB通路的激活相关.